Relationship between polymorphism of angiotensin-converting enzyme gene insertion/deletion and risk of hepatocellular carcinoma in a Chinese Dai population

J Renin Angiotensin Aldosterone Syst. 2015 Sep;16(3):695-9. doi: 10.1177/1470320314539829. Epub 2014 Sep 10.

Abstract

Introduction: The angiotensin-converting enzyme gene (ACE) is directly involved in the process of cancer cell proliferation, differentiation, apoptosis and angiogenesis. It also plays a vital role in inducing liver fibrosis and developing hepatocellular carcinoma (HCC). The aim of this study was to investigate the relationship between ACE insertion/deletion (I/D) polymorphism and the risk of HCC in a Chinese Dai population.

Materials and methods: We conducted a study including 210 patients with HCC and 206 healthy controls in Yunnan Cancer Hospital between January 2012-January 2014. I/D genotypes of ACE were determined with polymerase chain reaction (PCR) amplification of DNA from peripheral blood leukocytes.

Results: The ACE D allele was more frequent in the HCC cases than in the controls (51.7% vs 44.4%, p=0.036). Individuals with DD genotypes were associated with increased HCC risk compared with those with the II genotypes (odds ratio (OR), 1.911; 95% confidence interval (CI), 1.081-3.379; p=0.025). However, the ACE I/D polymorphism were not significantly associated with any clinicopathological characteristics such as the tumor stage, serum alpha-fetoprotein (AFP) level, and hepatitis B virus (HBV) infection.

Conclusions: The DD genotypes of ACE I/D polymorphism might contribute to the prediction of HCC risk in a Chinese Dai population.

Keywords: Hepatocellular carcinoma; angiotensin-converting enzyme; polymorphism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Asian People / genetics*
  • Carcinoma, Hepatocellular / enzymology
  • Carcinoma, Hepatocellular / genetics*
  • Ethnicity / genetics
  • Female
  • Genetic Predisposition to Disease*
  • Humans
  • INDEL Mutation / genetics*
  • Liver Neoplasms / enzymology
  • Liver Neoplasms / genetics*
  • Male
  • Middle Aged
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic*
  • Risk Factors
  • Young Adult

Substances

  • ACE protein, human
  • Peptidyl-Dipeptidase A